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莫申颗粒通过通过基碳化合物受体信号传递来调节NF-ƙB/Nrf2通路来改善膜性病

Shi-Xing Ma¹, Xiao-Jun Li², Ting-Ting Duan³

¹Department of Nephrology, Baoji Central Hospital, Baoji, Shaanxi 721008, China.

|October 9, 2023

概括

莫申颗粒 (MSG) 减少蛋白尿症,通过抑制基碳化合物受体 (AHR) 信号传递,从而减少氧化应激和炎症,改善异常性膜性病 (IMN) 中的功能.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
药理学药理学是指药理学的学科.
分子生物学分子生物学

背景情况:

异形膜性病 (IMN) 是成年人性综合征的主要原因.
目前对IMN的治疗方法在阻止疾病进展方面缺乏有效性,需要新的治疗策略.
亚利碳化合物受体 (AHR) 激活与IMN特征的氧化应激和炎症有关.

研究的目的:

为了研究莫申颗粒 (MSG) 对异常性膜性脏病 (IMN) 的治疗效果.
阐明MSG作用背后的分子机制,重点关注酸受体 (AHR),核因子-卡帕B (NF-κB) 和核因子红色素2相关因子2 (Nrf2) 途径.

主要方法:

评估了MSG在IMN患者的疗效,并对一种由阴性牛血清白蛋白 (CBSA) 诱导的老鼠模型进行了评估.
量化了AHR,NF-κB,Nrf2的mRNA和蛋白质表达水平,以及它们在脏组织中的下游目标.

主要成果:

在IMN患者和CBSA诱导的老鼠中,MSG显著降低了蛋白尿和改善了功能.
多氨基糖抑制了AHR及其下游基因 (CYP1A1,CYP1A2,CYP1B1,COX-2) 的表达.
MSG降低了NF-κB信号传递 (p-IκBα,NF-κB p65,MCP-1,COX-2,12-LOX,iNOS,p47phox,p67phox),同时保持了Nrf2信号传递 (catalase,HO-1,GCLM,GCLC,MnSOD,NQO1) 的情况.

结论:

在IMN中,MSG通过抑制AHR介导的NF-κB激活和促进Nrf2-依赖的抗氧化途径,有效地减轻细胞损伤.
通过向氧化应激和炎症,MSG为治疗IMN提供了一个有希望的治疗候选者.

关键词:

阿里碳水化合物受体是什么?异常发病的膜性脏病.莫申花粉颗粒是什么意思 Nrf2 没有任何问题.核因子卡帕 B B 的核因子

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